Hyperlipidimia is one of the well-known coronary risk factor.Serum cholesterol ( Various fractions ) levels are measured to represent that risk. Epidemiologically ,it does a perfect job , however , the fact is , circulating lipids has little correlationwith the lipids that’s deposited in the vessel wall.

Time and again , we have proven this as severity of CAD has little to do with the absolute levels of lipid levels.The number volume of plaques , the thickness of lipid core, and degree of vulnerability show poor correlation with circulating lipid levels than what we would expect.It tempts us to make a statement , that serum lipid is a poor surrogate marker for CAD. (Still, it may predict the risk of developing it !)

Why this paradox ? What are the missing links and hidden secrets ?

If you plot a simple graph with serum lipids with plaque mass, volume and content in CAD population , we might get an answer .I don’t know whether such a study exist. (Those who find one , please share)

It was reported in one of the rare research paper that came from (Abela Am J Cardiol.2009) Factors that crysalise cholesterol include local saturation, PH, temperature , hydration and plaque RBC contact.

If you argue lipid levels are not correlating with CAD , how is that reducing it with statins dramatically reduce CAD and the events ?

Like blood pressure the normality of serum lipids itself is not defined.One insightful definition was proposed , that the level at which a person develops CAD is high for that patient however low it may be..A person who develops extensive CAD say at a level of 90mgLDL what to infer ? We do not know exact answer.

That’s why the concept of satin for all with clinical CAD looked attractive. Still , statin’s action doesn’t help answer the original query about the relationship between blood lipids and plaque lipids.

Statins beneficial effect is not by reduction of serum cholesterol.It primary acts by regressing intra-plaque lipids by blocking synthesis of lipids in every cell.The anti inflammatory,plaque stabilisation action of statin may be independent of lipid reduction.How much it contributes to overall benefits is not known.

The mystery will deepen

Not every LDL is bad.(I will be slapped if I call them Good LDL !) Small dense LDL , LDL P (Particle) ApoB (The real culprit on which LDL piggybacks ) lipoprotein little a and so many other lipid sub particles are being studied.

Final message

The purpose of this post is not to confuse our understanding about coronary lipidology but to widen our vision . Serum lipids remain a poor surrogate marker for plaque lipids. This is because , It’s rather a small fraction of sample volume we catch in the circulating blood , while loads of lipids gets deposited elsewhere in the body ! This also make it clear,no single risk factor in isolation is really CAD risky.It is the combination of risks , genetic susceptibility , LDL subfractions, few unknown risk/protective factors and finally a mandatory trigger(Hemodynamic, Emotional ?) that determine the outcome of CAD.

So ladies and gentle men , just don’t over react to mildly abnormal lipid levels you often find in master health checks .There is much more untold stories behind the true CAD risk than the glossy lab printouts would suggest !

Avoid all Inotropics ( Doubutamine and Milrinone were shown to improve quality of life marginally but with dramatic reduction in quantity of life ! However , the same thing does not apply for Digoxin as it is the the only Inotropic with a soothing para-sympathetic comfort !

When a patient comes with angina at rest , it could mean two things .Either a STEMI or an NSTEMI .This , we can diagnose only after seeing the ECG .

Can we differentiate these two by the character of chest pain alone ?

Very tough task isn’t ? But there are some definite clues .

Infarct pain

Is mostly sudden .

Likely to be crescendo , lasts more than 20-30 minutes .

Fails to get relived by rest or even Nitrites.

Sweating due to sympathetic activation is more pronounced.

Unstable angina

Is rarely sudden .Often has a pro-drome.

UA is mostly precipitated by an increased demand situation or a stress.

It has a typical waxing and waning pattern . Rarely assume a true crescendo character as myocytes does not necrose (Just threaten to die !)

The chest pain radiation to shoulder is less conspicuous , instead it tends to reach the jaw area .(* An observation,Is it something to do with multi-vessel CAD in UA ?)

Mechanism of the difference : Epicardial vs Endocardial angina

The pain of UA is due to subtotal occlusion and endocardial ischemia , while STEMI is sudden total occlusion and the resultant transmural ischemia . In STEMI epicardial surface is always involved (Which lifts the ST segment in ECG .).We know epicardium is same as visceral layer of pericardium which is well innervated .Hence pain of STEMI acquires more of somatic character than a predominately visceral type pain that occurs with UA/NSTEMI where epicardial ischemia is absent.

Clinical importance

The demarcation between unstable angina and Infarct pain becomes vital when we calculate the time window for thrombolysing STEMI .Many of them have a phase of pre infarction angina which is a type of unstable angina. If we mistake it for Infarct pain then one may falsely calculate a prolonged time window and deny re-perfusion therapy.

Post -amble

It is tricky issue to differentiate the chest pain of STEMI and NSTEMI .A significant overlap can occur in real coronary care scenario . We know chest pain that occurs in both pre and post infarct phase is considered as unstable angina .(With infarct pain sandwiched between them!) Hence differentiating them may even be termed as futile.

Still,clinical cardiology can be made fascinating by indulging in such exercise !